Role of Stress Protein on Bacterial Infection

应激蛋白在细菌感染中的作用

• 批准号: 08670317
• 负责人: YAMAMOTO Tomoko
• 金额: $ 1.47万
• 依托单位: Kyorin University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1996
• 资助国家: 日本
• 起止时间: 1996 至 1998
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-08670317/
• 关键词: stress protein; bacterial virulence; macrophage; Y.enterocolitica; L.monocytogenes; phagocytosis; シャペロン; 病原性; エルシニア; リステリア; 細菌病原因子

All organisms respond to unfavorable conditions such as stressful environment by the rapid and transient acceleration in the synthesis of a group of proteins called the stress proteins. For pathogenic bacteria, the intracellular environment of macrophages is one of the most hostile environments. Therefore, the bacteria in the phagocytes may respond to the hostile stimuli by the expression of the stress proteins, and those pro. teiris may put the intracellular bacteria at advantages in the survival in the phagocytes. To elucidate the role of bacterial stress protein on the survival in the macrophages and expression of virulence, we studied the stress response and the role of stress proteins of Yersinia enterocolitica and Listeria monocytogenes within macrophages after phagocytosis. The results are as follows ; (1) The Y.enterocolitica gsrLAMBDA was identified as essential for protecting cells under both extracellular environmental stress and intracellular stress in macrophages due to phagocytosis. The gsrLAMBDA encodes a basic 49.5 kDa protein which is a periplasmic protease. (2) The GsrA stress protein was induced by macrophage phagocytosis. (3) L.monocylogenes could grow in macrophages without the induction of stress proteins. (4) The dnaK gene was cloned and subjected to the molecular analysis to understand the role of stress protein DnaK for intracellular survival of L.monocylogenes . (5) The DnaK does not largely contribute to the survival of L.inonocytogenes in macrophage cells but is involved in the step of the phagocytosis. From these results, it is speculated that common mechanisms with the stress proteins would contribute to the expression of the bacterial pathogen esis besides the species-specific mechanisms.

所有生物体都会通过快速、短暂地加速一组称为应激蛋白的蛋白质的合成来对不利条件（例如应激环境）做出反应。对于病原菌来说，巨噬细胞的细胞内环境是最恶劣的环境之一。因此，吞噬细胞中的细菌可能通过表达应激蛋白和亲应激蛋白来对敌对刺激做出反应。 Teiris 可能使细胞内细菌在吞噬细胞中处于生存优势。为了阐明细菌应激蛋白对巨噬细胞存活和毒力表达的作用，我们研究了小肠结肠炎耶尔森氏菌和单核细胞增生李斯特氏菌吞噬后巨噬细胞内的应激反应和应激蛋白的作用。结果如下； (1) 小肠结肠炎耶尔森氏菌 gsrLAMBDA 被确定为在细胞外环境应激和巨噬细胞因吞噬作用而产生的细胞内应激下保护细胞所必需的。 gsrLAMBDA 编码基本的 49.5 kDa 蛋白质，它是一种周质蛋白酶。 (2)GsrA应激蛋白由巨噬细胞吞噬诱导。 (3)L.monocylogenes无需应激蛋白诱导即可在巨噬细胞中生长。 (4)克隆dnaK基因并进行分子分析，了解应激蛋白DnaK对单核细胞胞内存活的作用。 (5)DnaK对巨噬细胞中李斯特氏菌的存活贡献不大，但参与了吞噬作用的步骤。根据这些结果，推测除了物种特异性机制之外，应激蛋白的共同机制也将有助于细菌病原体esis的表达。

项目成果

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山本 友子: "細菌の食菌抵抗性とストレス蛋白質" 医学のあゆみ. 178. 446-447 (1996)

Tomoko Yamamoto：“细菌食物抗性和应激蛋白”医学史 178. 446-447 (1996)。

Yamaguchi H et al.: "Analysis of the epitopes recognized by mouse monoclonal antibodies directed to Yersinia enterocolitica heat-shock protein 60." Microbiol.Immunol.40. 77-80 (1996)

Yamaguchi H 等人：“针对小肠结肠炎耶尔森氏菌热休克蛋白 60 的小鼠单克隆抗体识别的表位的分析。”

T.Yamamoto, T.Hanawa, S.Ogata & S.Kamiya: "Idcntitication and characterization of the Yersinia enterocolitica gsr Agene which protectivelyresponds to intracellular stress induced by macrophagc-phagocytosis and to extracellular environmental stresses." Inf

T.山本、T.花轮、S.绪方

Tomoko Yamamoto, Tomoko Hanawa and Shigeru Kamiya: "The Yersinia enterocolitica GsrA protein, involved in intracellular survival, is induced by macrophage-phagocytosis" Infect.Immun. 65. 2190-2196 (1997)

Tomoko Yamamoto、Tomoko Hanawa 和 Shigeru Kamiya：“小肠结肠炎耶尔森氏菌 GsrA 蛋白参与细胞内存活，由巨噬细胞吞噬作用诱导” Infect.Immun。